Objective: To verify the health advisory for short-term exposure to phenol. Methods: The method of this validation experiment was the same as the US Environmental Protection Agency (EPA) methodology for toxicology experiments used to determine phenol drinking water equivalent level (DWEL). Pregnant female Sprague-Dawley rats were administered phenol in distilled water by gavage at daily doses of 15, 30, 60, 120, and 240 mg/kg body weight (b.w.) from implantation (the 6th day post-mating) to the day prior to the scheduled caesarean section (the 20th day of pregnancy). The following information was recorded: general behavior; body weight; number of corpus luteum, live birth, fetus, stillbirth, and implantation; fetal gender; body weight; body length; tail length; and abnormalities and pathomorphological changes in the dams. Results: In the 60 mg/kg b.w. dose group, the mortality of pregnant rats increased with increasing doses, suggesting maternal toxicity. Fetal and placental weights decreased as phenol dose increased from 30 mg/kg b.w., and were significantly different compared those in the vehicle control group, which suggested developmental toxicity in the fetuses. However, the phenol-exposed groups showed no significant change in other parameters compared with the vehicle control group ( > 0.05). Conclusion Despite using the same method as the US EPA, a different NOEAL of 15 mg/(kg·d) was obtained in this study.
Animals ; Dose-Response Relationship, Drug ; Environmental Pollutants ; toxicity ; Female ; Fetal Development ; drug effects ; Phenol ; toxicity ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Toxicity Tests, Acute

An accidental spill of phenol (100%) into the Nakdong river with subsequent contamination of the tap water for about two million consumers in Teagu city of Korea occurred in March 1991. A historical cohort study of 6,913 individuals was undertaken to determine association with illness. Population subjects were divided into two groups of exposed and unexposed. Exposed subjects were reported to have significantly more phenol associated symptoms than those in a nearby unexposed area (39.6% vs. 9.4%, p < 0.01). Especially, in the related symptoms, highly significant differences were noted in the number of subjects reporting gastrointestinal illness such as nausea, vomiting, diarrhea, or abdominal pain. During the accident, study subjects who experienced peculiar taste or odor in the tap water were significantly more in the exposed areas (92% vs. 34.3%).
*Accidents ; Adolescent ; Adult ; Aged ; Child ; Child, Preschool ; Cohort Studies ; Female ; Human ; Infant ; Infant, Newborn ; Male ; Middle Age ; Phenol ; Phenols/*toxicity ; Water Pollutants, Chemical/analysis/*toxicity ; Water Supply/*analysis

The detrimental effects of environmental pollutants on the health of the individual are generally accepted, although the mechanisms of these effects remain to be incompletely understood. In the present study, we examined the effects of B[a]P, 2-BP, phenol and TCDD on proinflammatory cytokine gene expression in mice spleen cells which were stimulated with anti-CD3. 10-9M TCDD increased IFN gammar and TNF alpha gene expression, but suppressed IL-1 gene expression. 10-6M phenol inhibited IL-1, IL-6 and TNF alpha gene expression, and 10-6M of 2-BP downregulated TNF alpha gene expression. However, 10-6M of B[a]P did not influence on IL-1, IL-6, IFN gammar and TNF alpha gene expression. These findings suggest that TCDD may impair the immune functions of mice by enhancing proinflammatory cytokines production, whereas phenol and 2-BP may impair the functions by inhibiting the production of these cytokines.
Animals ; Antigens, CD3/immunology ; Apoptosis/drug effects ; Benzo(a)pyrene/*toxicity ; Cells, Cultured ; Cytokines/*biosynthesis/genetics ; Environmental Pollutants/*toxicity ; Gene Expression/drug effects ; Hydrocarbons, Brominated/*toxicity ; Male ; Mice ; Mice, Inbred C3H ; Phenol/*toxicity ; RNA/chemistry/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Spleen/*drug effects/metabolism ; Tetrachlorodibenzodioxin/*toxicity